foreign bodies that are subject of the typical ironcontaining foreign body touching the eye in all types of metal processing professions. The process is an initial mechanical attachment of a hot and high surface metallic foreign body to the corneal or conjunctival surface. Next, an ionic dissolving of iron from the surface of the particle and under oxygen exposure on the eye surface leads to the formation of rust [19] that moves into the tissue and forms the typical aspect around the particles. This process might, if removal is delayed, result in complete dissolving of the particle and severe inflammation triggered by iron oxide [20].

Another foreign body that typically interferes in eye burns is calcium oxide in any form like fluid concrete to fresh mixtures of CaO (Calcium oxide) with water. The reactive CaO dissolves with the water being attracted from the eye into Ca++ with additional hydroxyl ions. The saponification of the tissues by the alkali results in the diffusion of the foreign body into the tissue with deep corneal foreign body, difficult to remove [21]. All other known bioactive foreign bodies usually, more or less, follow these two different reaction types.

5.2.2.4  Eye Burns with Chemically Reactive Fluids

Alkali

Alkali is a frequent cause of eye burns as again confirmed in a recent study of Midelfarth [22]. Alkali reacts with the tissue surface by concentration and time-dependent dissolution of the lipid membranes of epithelial cells; the chemical mechanism is saponification of lipids with loss of all membranous barriers. Lipid saponification of membranous lipids starts at a pH over 11 [23].

The penetration into the tissue follows the initial breakdown of the epithelial barrier. This results in an immediate and strong edema of the conjunctiva, known as chemosis, due to a water influx from the surrounding tissue, vascular leakage, tears, and applied fluids. The cornea itself loads up with ions to a measured osmolarity of 1,830 mOsmol/kg after a 1 mol NaOH burn for 30 s [24]. The penetration of strong alkali has been systematically tested on sodium hydroxide by means of evaluation of the anterior chamber pH. This pH change typically occurs within 2 min after exposure of the corneal surface. The change of the cornea

shows immediate swelling of the corneal tissue in an order of magnitude of 20%, as published by Kompa et al in 2000. Increasing opacity of the cornea is a result of the tissue edema and of the change of the fibrillary structure of the collagen.

Acids

Acids act on the organic tissues when in a range of pH under 5. The free hydrogen ion is highly reactive and causes severe coagulation of proteins with superficial and deep ulceration if the excess of acid is high enough. The propagation of acids into the tissue is less fast than that of alkali. In case of hydro sulfuric acid, we found very fast propagation of the acid into the anterior chamber. We believe that in highly concentrated acids, the shrinkage of the tissue allows faster diffusion [25].

Peroxides

Peroxides react by free electron transfer from one molecule to the next. This gives typically slower damage characteristics. The body is quite used to decontaminate free radicals by means of the superoxide dismutase [26]; the system consists of glutathione, tocopherol, and ascorbic acid with its regeneration by means of the glutathione peroxidase. Further, the enzyme catalase is highly reactive toward hydrogen peroxide and its decontamination [27]. If this system is exhausted, the damage of any chemical structure results in membrane lysis, DNA strain breaks, and protein damage; this causes a delayed onset of necrosis which is commonly known on the eye of contact lens wearers forgetting to neutralize their 3% hydrogen peroxide containing cleaning solutions. The onset of symptoms is late, from 6 h to 3 days after exposure, being proven by Maurer et al. [28] in their experimental exposure on rabbits (Fig. 5.13).

Sometimes severe damage of the cornea can occur [29, 30]. The conjunctival damage is mostly low due to the good vascularization and fast repair by means of blood refilling of the protective mechanisms.

We found severe endothelial and stromal damage after exposure to hydrogen peroxide with a defined 10 mL exposure of a 7 mm diameter on the cornea in the EVEIT model. These exposures lead in all cases to a dose-dependent endothelial dysmorphy in lower

Fig. 5.14  Epithelial healing after exposure to H2O2

Fig. 5.15  Endothelial defects of ex vivo corneas at different time points after exposure to various concentrations of H2O2